The neuroanatomical substrate of hypothalamic hyperphagia and obesity is being explored. The VMH lesion syndrome consists of hypoactivity, hyperinsulinemia, polydipsia, hypergastric acidity, stunted linear growth and finickiness in addition to the hyperphagia and obesity. Using selective knife cuts and fiber of passage sparing lesions we have demonstrated that several of the above symptoms are due to coincidental brain damage, whereas others are an integral part of the syndrome.